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目的:研究槲皮素对野百合碱(MCT)诱导的肺动脉高压大鼠肺动脉平滑肌细胞增殖和肺动脉结构重建的调节作用。方法:成年雄性SD大鼠40只随机分为4组:正常对照组(对照组)、MCT诱导的肺动脉高压组(MCT组)、槲皮素预防组(预防组)和槲皮素治疗组(治疗组),每组10只。测量各组大鼠干预后平均肺动脉压力(mPAP);测定肺小动脉管壁厚度(WT)占动脉外径(ED)的百分比(WT%)及管壁面积(WA)占血管总面积的百分比(WA%);采用免疫组化和Western blot检测肺小动脉平滑肌细胞增殖细胞核抗原(PCNA)和平滑肌细胞抗体(α-SMA)的表达。结果:野百合碱组50mg/kg,再以生理盐水2ml/d每日灌胃一次,共20天,与对照组(生理盐水,再以生理盐水2ml/d每日灌胃一次,共20天)、预防组(MCT 50mg/kg,同时给予槲皮素100mg/kg每日灌胃一次,共20天)和治疗组(MCT 50mg/kg饲养20天后,以槲皮素100mg/kg每日灌胃一次,共20天)相比,mPAP、WT%、WA%、PCNA阳性率显著升高及PCNA、α-SMA的表达显著增多。结论:槲皮素对野百合碱诱导的大鼠肺动脉高压有预防和治疗作用,其机理可能是通过抑制肺血管中小动脉平滑肌细胞增殖,改善肺血管重构。
AIM: To investigate the regulatory effect of quercetin on pulmonary artery smooth muscle cell proliferation and pulmonary structural remodeling induced by monocrotaline (MCT) in rats. Methods: Forty adult male Sprague-Dawley rats were randomly divided into 4 groups: normal control group (MCT group), MCT group, quercetin preventive group (preventive group) and quercetin treatment group Treatment group), 10 in each group. The mean pulmonary arterial pressure (mPAP) was measured after intervention in each group. The percentage of pulmonary arteriole wall thickness (WT) to arterial diameter (ED) and the percentage of wall area (WA) (WA%). The expressions of proliferating cell nuclear antigen (PCNA) and smooth muscle cell antibody (α-SMA) in pulmonary arterioles were detected by immunohistochemistry and Western blot. Results: monocrotaline group 50mg / kg, and then with saline 2ml / d gavage once a day for 20 days, and the control group (normal saline, then saline 2ml / d once daily for 20 days ), Preventive group (MCT 50mg / kg, simultaneous administration of quercetin 100mg / kg once daily for 20 days) and treatment group (MCT 50mg / kg after 20 days of feeding, with quercetin 100mg / kg daily irrigation Stomach once, a total of 20 days) compared to mPAP, WT%, WA%, PCNA positive rate was significantly increased and PCNA, α-SMA expression was significantly increased. CONCLUSION: Quercetin can prevent and treat pulmonary hypertension induced by monocrotaline in rats. The mechanism may be that it can improve pulmonary vascular remodeling by inhibiting the proliferation of SMMCs in the pulmonary arteries.